Local and systemic factors can affect the survival rate of dental implants [30–33]. The causes of early implant failure are not fully clarified and an association between vitamin D and dental implant osseointegration has not been investigated properly [8, 13–16]. Some recent animal studies in rodents demonstrated a relationship between vitamin D supplementation and an increased bone to implant contact/volume after implant placement [14, 34, 35]. Mengatto et al. demonstrated an impaired osseointegration in vitamin D-deficient rats [36]. Other authors cannot confirm an effect of vitamin D supplementation on bone formation around titanium implants in diabetic rats [37]. A combination of local or systemic calcium supplementation and vitamin D seems to influence bone regeneration in extraction sockets of the dog as it demonstrates significantly higher bone formation and bone density and significantly less vertical ridge reduction in contrast to sockets without supplementation [38, 39]. However, a present human study cannot confirm an effect due to vitamin D supplementation on bone formation or graft resorption after maxillary sinus augmentation [40]. Satue et al. found a positive influence of 7-dehydrocholesterol (7-DHC), the precursor of vitamin D, coated implants on osteoblast differentiation in vitro [41]. But whether vitamin D-coated dental implants have an effect of osseointegration in vivo is still unclarified [42].

In dental implantology, vitamin D has been investigated almost exclusively as influencing factor of the bone to implant contact and implant stability [17]. Vitamin D demonstrates several effects on bone metabolism: it upregulates the gene expression of osteocalcin, osteopontin, calbindin, and 24-hydroxylase, increases extracellular matrix protein formation by osteoblasts, and stimulates osteoclast activity [15, 43]. But beyond modulation of bone formation, vitamin D has an impact on the innate and adaptive immune response in the field of osteoimmunology and could therefore influence early implant healing [19, 44–49].

Bone necrosis during implant bed preparation or placement is considered as a reason for early implant failures [7, 8]. An additional vitamin D deficiency might disrupt the sensitive balance between the immune system and bone metabolism during implant healing due to direct or indirect alteration of osteoclast function. For instance, the removal of bone debris through osteoclasts could be hampered since vitamin D controls osteoclast precursor monocyte migration [50]. On the other hand, in vitro studies demonstrated that vitamin D inhibits dendritic cell maturation and function as well as T cell proliferation and influences B cell responses, inhibiting proliferation and plasma cell differentiation [51–54]. An altered cytokine release by immune cells caused by a low vitamin D level could lead to a dysregulation of osteoclast activation and differentiation via associated immunoreceptors in osteoclasts [55].